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Year 1 Semester 2 > Muscle Cells > Flashcards

Muscle Cells Flashcards

1
Q

Skeletal Muscle functions

A
  • Body movement
  • Body posture
  • Support and protection
  • Sphincter control
  • Temperature regulation
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2
Q

Smooth muscle functions

A
  • Sphincter control
  • Movement of food along GIT
  • Regulation of blood flow
  • Temperature regulation
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3
Q

Cardiac muscle functions

A

Regulation of blood flow

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4
Q

Characteristics of all muscles

A
  • Excitability: responsive to stimuli
  • Contractility: ability to shorten forcibly when adequately stimulated
  • Extensibility: can extend beyond their resting/relaxed length
  • Elasticity: recoil and resume its resting length after stretching
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5
Q

Common features of all muscle

A
  • Actin and myosin
  • Use of ATP
  • Calcium ions
  • Stimulation from action potential
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6
Q

Name the three types of troponin

A
  • Troponin T - binds to tropomyosin
  • Troponin C - binds to calcium
  • Troponin I - inhibitory aspect, binds to actin to prevent myosin binding
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7
Q

Name the three types of troponin

A
  • Troponin T - binds to tropomyosin
  • Troponin C - binds to calcium
  • Troponin I - inhibitory aspect, binds to actin to prevent myosin binding
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8
Q

Actin and myosin

A
  • Make up roughly 90% of muscle protein

- Both are ATPases and so hydrolyse ATP

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9
Q

Name for muscle cell membrane

A

Sarcolemma

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10
Q

Name for muscle cell cytoplasm

A

Sarcoplasm

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11
Q

Name for muscle cell endoplasmic reticulum

A

Sarcoplasmic reticulum

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12
Q

Name for a single muscle cell

A

Myocyte or myofibre

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13
Q

What are the connective tissues that cover and support skeletal muscle?

A
  • Epimysium
  • Perimysium
  • Endomysium
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14
Q

Define fasicle

A

Grouping of elongated bundles of muscle fibres

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15
Q

Define sarcomere

A

Contractile unit of myofilaments

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16
Q

Features of cardiac muscle

A
  • Can contract without stimulation - auto-rhythmic
  • Involuntary muscle - autonomic nervous system
  • Branched cells
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17
Q

Features of cardiomyocytes

A
  • Striated
  • Small - 100micrometres in length
  • Uni- or bi-nucleated
  • Intercalated discs: gap junctions and desmosomes
  • Large number of mitochondria
  • Aerobic respiration - can use multiple fuel sources
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18
Q

Features of smooth muscle cells

A
  • Small - 100 - 200 micrometres in length
  • Spindle shaped cells arranged into sheets
  • Less regularly organised
  • No striations
  • Single nucleus
  • Involuntary - ANS, hormones & stretch
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19
Q

How does smooth muscle contraction compare to the other types?

A

Slower contraction rate but longer duration

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20
Q

How does smooth muscle contraction compare to the other types?

A

Slower contraction rate but longer duration

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21
Q

What are T tubules?

A
  • extensions of the sarcolemma that invaginate into the cell
  • they transmit the electrical impulse deep within the cell structure
  • they are closely associated with the SR to stimulate release of Ca2+ - enables whole cell to contract almost simultaneously
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22
Q

Discuss the steps of muscle development

A
  • Embryonic mesoderm cells called myoblasts undergo cell division
  • Several myoblasts fuse together to form a myotube
  • Myotube matures into skeletal muscle fibre
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23
Q

What do Z discs form?

A

The boundaries between the sarcomeres

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24
Q

What are the supporting proteins critical for maintaining sarcomere structure?

A
  • alpha-actin
  • titin
  • nebulin
  • dystrophin
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25
Q

What is in the A band of a sarcomere?

A

Mainly myosin with some overlapping of actin

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26
Q

What is in the I band of the sarcomere?

A

Mostly actin

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27
Q

What binds the myosin to the M line?

A

Titin

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28
Q

Where is the M line

A

In the H zone of the A band

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29
Q

Sliding Filament Theory

A
  • At rest: the A band and I band are similar width
  • During contraction, the myosin binds actin, pulling inwards shortening the sarcomere - Z discs move closer together
  • The I band reduces in size
  • The A band remains the same width, consisting of greater actin and myosin overlap
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30
Q

What does each myosin-II molecule consist of?

A
  • Two intertwined heavy chains (MHC)
  • Two essential light chains (MLC-1) - stabilises myosin head
  • Two regulatory light chains (MLC-2) regulates ATPase activity of myosin
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31
Q

What covers the active site of actin to prevent contraction?

A

Tropomyosin

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32
Q

What is the role of calcium in skeletal muscle contraction?

A
  • Following neuronal stimulation and depolarisation of the muscle cell, Ca2+ is released from the SR and binds TnC
  • This causes conformational change in TnI and TnT rotates tropomyosin to reveal myosin binding sites on actin
  • In the presence of ATP, myosin can bind actin - sarcomeres shorten and muscle contracts
  • Calcium couples the electrical stimulation into mechanical contraction
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33
Q

Neuromuscular Junction

A

-Action potential travels down motor neurone to the terminal end plate/bouton
-Voltage gated calcium channels then open and an influx of Ca2+ initiates vesicles containing acetylcholine to fuse with membrane
-Acetylcholine (Ach) released into synaptic cleft
-Ach attaches to nicotinic Ach receptors (nAchR)
Acetylcholinesterase rapidly breaks down Ach in synaptic cleft

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34
Q

Full name for T tubules

A

Transverse tubules

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35
Q

End of Contraction

A
  • Action potential stops, Ca2+ is pumped back into the SR by active transport - sarco-endoplasmic reticulum calcium ATPase (SERCA)
  • Within the SR, calsequestrin and calreticulin are major Ca-binding proteins in skeletal muscle
  • Located predominantly at triad junction
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36
Q

Define excitation contraction coupling

A

Linkage between excitation of the muscle fibre membrane and the onset of contraction

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37
Q

What is the latent period in skeletal muscle contraction?

A

The time from the peak of the action potential to the onset of contraction

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38
Q

What causes the latent period in skeletal muscle contraction?

A

Changes in the electric field are restricted to the immediate vicinity of the plasma membrane and so other actions are required to reach all the muscle fibres causing a delay

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39
Q

What makes a triad?

A

Two terminal cisternae (part of the sarcoplasmic reticulum) and one T tubule

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40
Q

Role of the transverse tubule

A
  • Action potential is propagated from the end plate along the surface of the muscle fibre (sarcolemma)
  • Action potential is propagated into the fibre down the T-tubule membrane
  • Depolarisation of the T-tubule membrane is ‘signalled’ to the membrane of the terminal cisternae
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41
Q

Which 2 intracellular compartments is calcium recycled between?

A
  • Sarcoplasmic reticulum

- Cytoplasm

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42
Q

Name and explain the junctional foot proteins

A
  • Dihydropyridine receptor protein (DHPR): L-type voltage-gated calcium channel in the T-tubule membrane
  • Ryanodine receptor protein (RYR): calcium release channel in the SR
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43
Q

Explain the coupling system of the junctional foot proteins

A
  • Membrane depolarization opens the L-type Ca2+ channel (DHPR) causing a conformational change
  • Mechanical coupling between DHPR and RYR causes the RYR channel to open
  • Ca2+ exits the SR via the RYR and activates troponin C leading to muscle contraction
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44
Q

What is the change in calcium concentration during contraction?

A

from <10-7 to >10-5

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45
Q

What can be used to block dihydropyridines?

A

Voltage-gated Ca2+ channel blocking drugs such as Nifedipine

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46
Q

What is malignant hyperthermia?

A
  • Pharmacogenetic disorder of skeletal muscle
  • Severe reaction to commonly used anaesthetics and depolarising muscle relaxants
  • First manifestations of MH occur in the operating room
  • Fatal if untreated
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47
Q

Symptoms of malignant hyperthermia

A
  • Muscle rigidity
  • High fever
  • Increased acid levels in blood and other tissues
  • Rapid heart rate
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48
Q

What is the underlying mechanism of malignant hyperthermia?

A

Point mutations in the gene coding for Ryanodine receptor type 1 channels

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49
Q

What does SERCA stand for

A

Sarcoplasmic Endoplasmic Reticulum Calcium ATPase

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50
Q

Role of Ca2+ ATPase

A
  • The increase in intracellular calcium concentration activates a Ca2+ ATPase (calcium pump) in the SR membrane
  • Active transport of calcium from the cytoplasm into the SR (2 Ca2+ ions per molecule of ATP hydrolysed)
  • Ca2+ concentration decreases to <10-7M
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51
Q

Role of calsequestrin

A
  • Stores calcium at high concentrations in the terminal cisternae to establish a concentration gradient from the SR to the cytoplasm
  • Binds 43 Ca2+ ions per molecule
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51
Q

Role of calsequestrin

A
  • Stores calcium at high concentrations in the terminal cisternae to establish a concentration gradient from the SR to the cytoplasm
  • Binds 43 Ca2+ ions per molecule
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52
Q

What are pacemaker cells?

A
  • Specialised muscle cells
  • Unstable resting potential
  • Undergo automatic rhythmical depolarisation
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53
Q

What effects do the parasympathetic and sympathetic nervous system have on cardiac muscle?

A
  • Parasympathetic - slows the rate

- Sympathetic - increases rate and strength

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54
Q

What neurotransmitters are involved in each pathway that affects cardiac muscle?

A
  • Parasympathetic - acetyl choline

- Sympathetic - nor-adrenaline

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55
Q

What is the difference in the action potential between cardiac and skeletal muscle?

A

Cardiac action potential lasts a lot longer and the contraction response occurs during the action potential.

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56
Q

What is Ca2+-induced Ca2+ release in cardiac muscle?

A
  • 25% of the required Ca2+ enters through the L-type Ca2+ channels (DHPR) in the transverse tubular membrane
  • This triggers release of Ca2+ via the Ca2+ sensitive (ryanodine) channels in the SR
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57
Q

Where does the calcium come from in cardiac muscle contraction?

A
  • 25% enters through the DHPR L-type calcium channel to induce CICR
  • 75% through the calcium sensitive calcium release RYR protein in the SR
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58
Q

Are the DHPR calcium channel and RYR channel coupled in cardiac muscle?

A

No

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59
Q

What is used for calcium storage to reduce the size of the concentration gradient between the SR and the cytoplasm?

A

Calsequestrin

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60
Q

Explain relaxation in cardiac muscle

A
  • Requires a decrease in cytoplasmic Ca2+ concentration from >10-5M to <10-7M
  • Ca2+ATPase in sarcoplasmic reticulum is activated
  • Ca2+ATPase in the cell membrane pumps out the trigger Ca2+
  • Na+:Ca2+ exchange in the sarcolemmal membrane (3:1)
61
Q

Which type of RYR is in each muscle type?

A
  • Type 1 in Skeletal

- Type 2 in Cardiac

62
Q

Explain the role of ATP in muscle

A
  • Membrane potential: Na+/K+ ATPase in sarcolemma maintains Na+ and K+ gradients, allowing production and propagation of action potentials
  • Ca2+ gradient: active transport of calcium ions into the sarcoplasmic reticulum - lowering [Ca2+]
  • Power stroke: hydrolysis of ATP by myosin-ATPase energises the cross-bridge formation enabling sarcomere shortening & contraction
  • Cross-bridge dissociation: binding of ATP to myosin dissociates cross-bridge bound to actin
63
Q

How can energy be stored in muscle cells?

A

ATP will donate its Pi to creatine forming ADP and creatine phosphate. When energy levels are low, a creatine kinase is used to produce ATP and creatine providing more energy.
These stores of CP in muscle provide enough energy for about 8 seconds of contraction.

64
Q

How do skeletal muscles get their energy?

A
  • Creatine phosphate: rapid ATP formation at the onset of muscle contraction
  • Glycolysis: anaerobic (fast rate of ATP generation from glucose/glycogen for about 1 minute)
  • Oxidative phosphorylation: aerobic (supplies most amount of ATP per glucose molecule (and other fuel types) and powers contraction for hours)
65
Q

Describe cross bridge formation and the power stroke

A
  • ATP binding releasing myosin from actin
  • ATP is hydrolysed causing a conformational shift so that myosin can aline to bind with the actin again
  • cross-bridge is formed
  • release of Pi, from myosin increasing strength of bond
  • power stroke
  • ADP release
66
Q

What affects the regulation of cross bridge formation?

A

Availability of myosin binding sites on actin, via [Ca2+], and tropomyosin

67
Q

What is rigor mortis?

A
  • Rigor mortis refers to the muscular stiffness that occurs after death - post-mortem rigidity
  • Can begin roughly 4 hours after death, peas at about 13 hours and lasts about 50 hours
68
Q

Process causing rigor mortis

A
  • Death
  • Ca2+ pumps no longer function
  • Ca2+ leaks into the cytosol from SR
  • Ca2+ binds to tropomyosin
  • Myosin binds to actin
  • ATP production ceases
  • No ATP present to break cross-bridges
  • Muscles become stiff
  • Proteolytic enzymes work within a few days
69
Q

What myosin type is most common in muscle cells?

A

Type 2

70
Q

What are the 3 types of myosin isoforms?

A
  • Type I
  • Type IIA
  • Type IIB/IIX
71
Q

How does the number of certain myosin isoforms affect the colour of muscle?

A

Muscle more red - more type I fibres, muscles more white - more type IIB/IIX

72
Q

What twitch speed is each fibre type?

A
  • Type I - slow
  • Type IIA - intermediate
  • Type IIB/IIX - fast
73
Q

What determines twitch speed of a muscle fibre?

A

The speed at which myosin is able to hydrolyse ATP

74
Q

What feature of a muscle fibre causes the difference in its colour?

A

The amount of myoglobin oxygen available. More myoglobin - muscle more red, less myoglobin - muscle lighter

75
Q

How does each fibre type tend to generate its ATP?

A
  • Type I - oxidative (aerobic)
  • Type IIA - mixture of fast oxidative and glycolytic
  • Type IIB/IIX - glycolytic (anaerobic)
76
Q

What features of the muscle cell are dependent on the fibre type?

A
  • Number of mitochondria
  • Amount of myoglobin (colour)
  • Blood vessels/capillaries
  • Stores of glycogen/glycolytic enzymes/creatine phosphate
  • Size
77
Q

In relation to contraction velocity, what is another feature of muscle affected by its fibre types?

A

Duration of contraction

78
Q

What are motor units:

A
  • A sigle motor neurone innervates multiple muscle fibres
  • All fibres innervated by a single neurone are called a motor unit
  • Generally - small muscles with fine control have more nerve fibres for fewer muscle fibres
  • Conversely large muscles may have hundreds of fibres in a motor unit
79
Q

What affects force of muscle contraction?

A
  • Number of motor units recruited

- Frequency of action potentials

79
Q

What affects force of muscle contraction?

A
  • Number of motor units recruited

- Frequency of action potentials

80
Q

What is the motor unit recruitment size principle?

A

Motor units recruited in a progressive way, from small (weakest) to large (strongest)

81
Q

Describe some features of small motor units

A
  • Innervate the fewest number of muscle fibres
  • More excitable
  • Conduct action potentials more slowly
  • Typically type I (slow) fibres
82
Q

Describe some features of large motor units

A
  • Less excitable
  • Conduct action potentials more rapidly
  • Typically type II (fast) fibres
83
Q

Define muscle tension

A

The force exerted by a contracting muscle

84
Q

Define load

A

The force exerted by an object to be moved - muscle must overcome this in order to shorten

85
Q

Explain the summation of muscle fibres

A
  • One action potential (AP) leads to a single skeletal muscle twitch (lasts from 25-200msec)
  • As muscle twitch exceeds duration of AP it is possible to initiate a second AP before 1st contraction has subsided - 2nd twitch stronger. than first due to higher [Ca2+] - summation
  • Multiple APs occuring close together - frequency summation
  • Tetanus - stimulation frequency so high that individual contractions fuse
86
Q

What is multi-unit smooth muscle?

A
  • Discrete separate fibres with own nerve ending - independent contraction
  • Mainly innervated by nerve signals
  • E.gs: ciliary muscle of the eye; iris; pilorector muscles; vas deferens
87
Q

What is unitary (or single unit) smooth muscle?

A
  • Sheets of electrically coupled cells - syncytium or visceral smooth muscle
  • Contract in unison
  • Connected by gap junctions
  • E.gs: GI tract, bile duct, ureters, uterus & blood vessels
88
Q

Describe the structure of smooth muscle

A
  • No striations: actin and myosin filaments arranged diagonally along fibres - less regularly organised
  • Dense bodies correspond to Z discs - lattice-like structures anchoring actin within the fibre and tethers contractile proteins to the sarcolemma
  • Dense bodies: composed of intermediate filaments (alpha-actin/desmin/vimentin) - transmit force of contraction within and between cells
89
Q

Describe some features of smooth muscle

A
  • Gap junctions - electrically couple cells in unitary smooth muscle
  • Focal adhesions - connect cells together mechanically
  • No troponin - regulation of smooth muscle contraction differs to both skeletal and cardiac muscle
  • No T tubules
  • The sarcoplasmic reticulum is much less developed
90
Q

Define caveolae

A

Pouchlike infolding of the sarcolemma - contain large numbers of Ca2+ channels because extracellular Ca2+ is the main trigger for contraction

91
Q

What cause the excitation contraction coupling in smooth muscle?

A

Influx of Ca2+ sourced from sarcoplasmic reticulum and/or extracellular Ca2+

92
Q

What are the three mechanisms that lead to an increase in [Ca2+]?

A
  • Voltage gated L-type Ca2+ channels: leading to calcium induced calcium release (CICR) via ryanodine receptor activation
  • Receptor operated Ca2+ channels: (RPCC) leading to IP3 receptor activation and CICR
  • Store operated Ca2+ channels (STOC)
93
Q

Myosin in smooth muscle

A
  • Myosin: tertiary structure similar to skeletal/cardiac, however some differences
  • Different amino acid sequence
  • Different arrangement of myosin head: along the entire length of molecule, head hinges opposing direction on the same filament - pulls in opposite directions, increasing shortening
94
Q

Actin in smooth muscle

A
  • Called smooth muscle actin

- 2 types: alpha-SMA (vascular) and gamma-SMA (GI tract)

95
Q

What is calmodulin?

A

Key regulatory protein enabling myosin to interact with actin

96
Q

How is myosin activated in smooth muscle?

A

Ca2+ binds to calmodulin allowing calmodulin to form a complex with myosin light chain kinase which then phosphorylates myosin allowing it to bind with actin to form cross bridges

97
Q

What has to happen to allow relaxation of smooth muscle?

A

Myosin must be dephosphorylated

98
Q

Describe the smooth muscle contraction process

A
  • Initiated by calcium influx from extra cellular fluid and SR
  • Calcium binds to calmodulin
  • Ca-calmodulin-MLCK complex leads to phosphorylation of MLC (requires 1ATP per MLC)
  • Phosphorylated myosin head binds to actin and power stroke occurs automatically
  • A second ATP is required to release myosin head from actin
99
Q

Describe the smooth muscle relaxation process

A

-When stimulus ends, calcium is pumped out of the cell or into SR
-When calcium drops below a critical level, calcium dissociates from calmodulin (inactivates MLCK)
Myosin phosphatase removes phosphate from the MLC , causing detachment of the myosin head from the actin filament, causing relaxation
-Timing of relaxation is determined by amount of active myosin phosphatase in cells

100
Q

How is calcium transported out of the sarcoplasm-extracellular fluid or into the SR in smooth muscle?

A
  • Membrane Ca2+ATPase (active)
  • Ca2+ATPase (SERCA) (active)
  • Na+-Ca2+ exchangers (passive)
101
Q

What are the mechanisms in place to ensure sufficient calcium is returned to the SR in smooth muscle?

A
  • Stim1 senses calcium levels in SR and activates store-operated Ca2+ channels (SOCs) for influx of calcium back into the cell
  • This enables SR to refill
  • This occurs at specialized regions where the SR encounters the sarcolemma
102
Q

Autonomic nervous system in smooth muscle

A
  • Unlike skeletal muscle, smooth muscle cell membranes contain receptors which can initiate or inhibit contraction
  • Smooth muscle lacks highly specialized neuromuscular junctions
  • Autonomic nerve fibres branch diffusely creating wide synaptic clefts - diffuse junctions
  • Swellings called variscosities release neurotransmitter in the general area of smooth muscle cells
103
Q

Variscosities in smooth muscle

A
  • Variscosities from a single axon may be located along several muscle cells
  • Variscosities originate from postganglionic fibres of both sympathetic and parasympathetic neurons
104
Q

What is the relationship between smooth muscle cells and neurotransmitters?

A

Several smooth muscle cells are influenced by neurotransmitters released by a single neuron, and a single smooth muscle cell may be influenced by neurotransmitters from more than one neuron

105
Q

What are the two key neurotransmitters involved in smooth muscle contraction?

A

-Acetylcholine
-Noradrenalin
(occasionally others)

106
Q

Aside from ANS what can regulate smooth muscle contraction?

A
  • Spontaneous electrical activity
  • Stretch
  • Hormones
  • Local chemicals within the extracellular fluid: oxygen, carbon dioxide, acidity, ion concentration, nitric oxide
  • Allows fine tuning of activity in response to environment
107
Q

What is the resting membrane potential of smooth muscle?

A

-50 to -60mV

108
Q

What can generate unitary smooth muscle spike potentials?

A
  • Electrical stimulation
  • Hormones
  • Stretch
  • Spontaneous depolarisation from pace maker cells (interstital cells) of the intestinal wall
109
Q

What is mainly responsible for membrane potential in smooth muscle?

A

Calcium - slower to open and close than Na+ channels

110
Q

Which tends to have a greater force of contraction, skeletal muscle or smooth muscle? Why?

A

Smooth muscle often has a greater force of contraction due to the longer cross bridge attachments between actin and myosin

111
Q

What is the latch mechanism in smooth muscle?

A

A mechanism which maintains prolonged contraction, with minimal ATP use - only 1 ATP required for each cycle

112
Q

When does the latch mechanism occur?

A

When myosin is dephosphorylated while still attached to actin (only if [Ca2+] remains elevated above background levels)

113
Q

What are the 3 ways to block neuromuscular transmission?

A
  • Presynaptically, by inhibiting ACh synthesis - rate-limiting step is choline uptake
  • Presynaptically, by inhibiting ACh release
  • Postsynaptically - by interfering with the actions of ACh on the receptor
113
Q

What are the 3 ways to block neuromuscular transmission?

A
  • Presynaptically, by inhibiting ACh synthesis - rate-limiting step is choline uptake
  • Presynaptically, by inhibiting ACh release
  • Postsynaptically - by interfering with the actions of ACh on the receptor
114
Q

What ways can ACh release be inhibited?

A
  • Local anaesthetics
  • General inhalational anaesthetics
  • Inhibitors/competitors of calcium - magnesium ions, some antibiotics such as aminoglycosides and tetracycline
  • Neurotoxins - Botulinium toxin (clostridium botulinum), beta-bungarotoxin
115
Q

Uses of botulinum toxin

A
  • Muscle spasticity treatment
  • Cosmetic uses
  • Reduce hyperhydrosis
116
Q

Why is botulinum toxin useful?

A

It doesn’t diffuse around the body and so can be locally used on certain muscles

117
Q

What are some clinical uses of neuromuscular blocking drugs?

A
  • Endotracheal intubation
  • During surgical procedures: to allow surgical access to abdominal cavity, to ensure immobility (e.g. prevent cough during head and neck surgery), allow relaxation to reduce displaced fracture or dislocation, decrease concentration of general anaesthetic needed
  • Infrequently in intensive care: mechanical ventilation at extremes of hypoxia
  • During electroconvulsive therapy
118
Q

Describe the nicotinic acetylcholine receptor

A
  • 5 transmembrane region (5 subunits)
  • A pore that allows the movement of sodium and potassium ions across the membrane of a cell when ACh binds to it and causes it to open
  • ACh must be bound to both binding sites to open the receptor allowing sodium to come in and some potassium to exit
118
Q

Describe the nicotinic acetylcholine receptor

A
  • 5 transmembrane region (5 subunits)
  • A pore that allows the movement of sodium and potassium ions across the membrane of a cell when ACh binds to it and causes it to open
  • ACh must be bound to both binding sites to open the receptor allowing sodium to come in and some potassium to exit
119
Q

What effect will an agonist have on nicotinic ACh receptors? Name some examples of agonists

A
  • An agonist will bind to the receptor and cause it to open.

- Examples are nicotine and suxamethonium

120
Q

What effect will an antagonist have on the nicotinic ACh receptor? Name some examples of an antagonist

A
  • Antagonists will bind to the binding site of the receptor and will not cause any conformational change resulting in the receptor remaining closed.
  • Examples are tubocurarine and atracurium
121
Q

What are the subunits that make up the nicotinic acetylcholine receptor at the neuromuscular junction?

A
  • 2 alpha subunits
  • 1 beta subunit
  • 1 gamma subunit
  • 1 delta subunit
122
Q

What are non-depolarising blockers?

A

Competitive antagonists of nicotinic ACh receptors at the NMJ

123
Q

What happens when a non-depolarising blocker binds to the receptor?

A
  • Prevents ACh binding to receptor by occupying site
  • Decreases the motor end plate potential (EPP)
  • Decreases depolarisation of the motor end plate region
  • No activation of the muscle action potential
124
Q

What are depolarising blockers?

A

Agonists of nicotinic ACh receptors at the NMJ

125
Q

What are depolarising blockers?

A

Agonists of nicotinic ACh receptors at the NMJ

126
Q

How is ACh degraded?

A

Acetylcholine esterase

127
Q

Why does suxamethonium stay bound to nicotinic ACh receptors?

A

It cannot be metabolised by acetylcholine esterase so it does not degrade

128
Q

What happens when suxamethonium binds to nicotinic ACh receptors?

A
  • Persistent depolarisation of the motor end plate
  • Prolonged EEP
  • Prolonged depolarisation of the muscle membrane
  • Membrane potential above the threshold for the resetting of coltage-gated sodium channels
  • Sodium channels remain refractory
  • No more muscle action potentials generated
129
Q

Describe the first phase of depolarising block using suxamethonium

A
  • Muscle fasciculations observed, then blocked
  • Repolarisation inhibited: K+ leaks from cells (hyperkalemia)
  • Voltage-gated Na+ channels kept inactivated
130
Q

Describe the second phase of depolarising block using suxamethonium

A
  • Prolonged/increased exposure to drug

- “Desensitisation blockade”: depolarisation cannot occur, even in absence of drug

131
Q

How to spot a non-depolarising blocker and which type it is

A
  • Non-depolarising blockers end in either -curonium or -curium
  • Ends in -curonium it’s an aminosteroidal
  • Ends in -curium it’s a benzylisoquiolinium
132
Q

What is a common side affect of aminosteroidals?

A

Tachycardia (high heart rate)

133
Q

What are common side affects of bensylisoquioliniums?

A

Hypotension and bronchospasm

134
Q

What are the main side affects of suxamethonium?

A
  • Bradycardia
  • Cardiac dysrhythmias
  • Raised intraocular pressure
  • Postoperative myalgia
  • Malignant hyperthermia
135
Q

How is atracurium degraded and removed from the body?

A

Ester hydrolysis and hofmann elimination

136
Q

What breaks down mivacurium and suxamethonium?

A

Plasma cholinesterases (takes longer to break down than acetylchloine esterase hence why suxamethonium can have the effect it does)

137
Q

Where are pancuronium and vecuronium broken down?

A

Liver

138
Q

How is rocuronium eliminated from the body?

A

Unchanged but eliminated by bile/urine

139
Q

How is the duration of action of ACh regulated?

A

Hydrolysis

140
Q

Describe acetylcholinesterase (ACh.E)

A
  • True cholinesterase, specific for hydrolysis of ACh
  • Present in conducting tissue and red blood cells
  • Bound to basement membrane in the synaptic cleft
141
Q

Describe plasma cholinesterase

A
  • Pseudocholinesterase, broad spectrum of substrates
  • Widespread distribution
  • Soluble in plasma
142
Q

What happens when anticholinesterase drugs are used?

A
  • Less degradation of ACh so more ACh available at NMJ
  • Increases duration of activity of ACh at NMJ
  • More ACh to compete with non-depolarising blockers
143
Q

Effects of anticholinesterases

A

Central nervous system:

  • Initial excitation with convulsions
  • Unconsciousness and respiratory failure

Autonomic nervous sytem:

  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • Gastrointestinal upset
  • Emesis
  • Bradycardia
  • Hypotension
  • Bronchoconstriction
  • Pupillary constriction
144
Q

Clinical uses of anticholinesterases

A

In anaesthesia:

  • Reverse non-depolarising muscle blockade
  • Given with atropine or glycopyrrolate to counteract parasympathetic effects

Myasthenia gravis:
-Increase neuromuscular transmission

Glaucoma:
-Decrease intraocular pressure

Alzheimer’s disease:
-Enhance the cholinergic transmission in the CNS

145
Q

What is myasthenia gravis?

A

Autoantibodies may be produced against the acetylcholine receptor blocking the interaction of the acetylcholine receptor with its ligand (acetylcholine) and leading to muscle weakness and death

146
Q

What is sugammadex and what does it do?

A
  • Selective relaxant biding agent (SRBA)

- Reverses effects of rocuronium and vecuronium

Year 1 Semester 2 (26 decks)

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